Human immunodeficiency virus (HIV) infection of humans and pathogenic simian immunodeficiency virus (SIV) infection of rhesus monkeys causes progressive immunocompromise and acquired immune deficiency syndrome (AIDS). One hallmark that correlates with the rate of progression to AIDS is systemic immune activation. Systemic immune activation is, in turn, associated with damage to the intestinal epithelium (enteropathy) and translocation of as-yet-undefined immunostimulatory pathogen-associated molecular patterns (PAMPS) or antigens into tissues and the blood.
Despite the importance of intestinal barrier damage to AIDS progression, the mechanisms responsible for AIDS enteropathy are not understood. One possibility is that immunodeficiency leads to epithelial damage by intestinal viruses or other pathogens. The mammalian virome and bacterial microbiome is extremely complex and can contribute to immune status and disease in a range of settings. Thus far, a prior study that utilized 16S rDNA sequencing, which was unable to detect viruses, found no discernible differences in the diversity of bacteria associated with SIV infection (McKenna et al., PLoS Pathog. 4: e20 (2008)). However, it remained a possibility that the virome, a subset of the metagenome that may be defined as viruses that infect eukaryotic cells, contributes to epithelial damage during lentiviral infection.
It is therefore important to understand the contribution of the virome to lentiviral infection-associated phenotypes, such as enteropathy. There is an unmet need in the field for understanding the contribution of the virome upon lentiviral infection, as well as for the development of alternative methods of diagnosing and treating lentiviral infections (e.g., HIV).